Infection is a key case of early death in patients with cirrhosis, precipitating 50% of hospital admissions (and among these, 15-35% develop a nosocomial infection) (Fernandez et al. Hepatology, 2012)

Sepsis and requirements for multi-organi support in the ICU is associated with a 65-90% mortality in this population (O’Brien et al. Intensive Care Med, 2012)

HCC and cirrhosis:

remember that HCC can give you MELD exception points to help get you listed for transplant. Transplant hepatologists use the Milan Criteria to determine suitability for liver transplant in these patients (people who don’t meet these criteria are at high risk of recurrent HCC post-transplant)

Single tumor <5cm in diameter, or up to 3 tumors, each < 3cm

No extrahepatic involvement

No major vessel involvement

Sometimes, patients’ tumors are too big and may benefit from locoregional treatment to reduce size of tumors. Options include:

Most common cause of death is neurological complications (edema and herniation). Hyperammonemia crosses the BBB and gets stuck, pulls in fluid and causes cerebral edema. Should go to the ICU for q1-2hr neuro checks, may need hypertonic saline and mannitol (targeted to Na 145 or Serum osm 320)

Differential for ALT >1000 is short with three main things: toxin (Tylenol, mushroom), ischemia, viral hepatitis

Ammonia:

Useless in end stage liver disease for hepatic encephalopathy. Must be made as a clinical diagnosis

Yesterday at M&M, nephrologist Dr. Lowell Lo was at it again – dropping serious knowledge. He presented his basic approach to finding protein in the urine. He said that his first step in evaluating proteinuria is to consider which of the four types he is dealing with.

The four basic types of proteinuria are:

Glomerular:

caused by increased filtration of macromolecules (e.g. albumin) across the glomerular capillary wall

in a normal kidney, low-molecular-weight proteins (smaller than albumin) get filtered across the glomerulus and are largely reabsorbed in the proximal tubule (examples include immunoglobulin light chains, beta-2-microglobulin)

diseases that cause tubulointerstitial damage limit reabsorption of these proteins in the proximal tubule, leading to proteinuria

increased excretion of these smaller proteins is often not detected on urine dipstick

the increased excretion of tubular proteins (e.g. polyclonal immunoglobulin light chains) is not injurious to the kidney